ArticleJournal of virology2013
Visualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1.
Article in Journal of virology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Animal Models for Swine Influenza Virus Research: Pathology, Viral Dynamics, and Immune Responses.Viruses · 2026Review
- Interferon-β induction heterogeneity during KSHV infection is correlated to levels and activation of the transcription factors ATF2 and RelA, and not IRF3.PLoS pathogens · 2026Article
- Influenza A virus-induced interferon-alpha production by myeloid dendritic cells and macrophages requires productive infection.Emerging microbes & infections · 2025Article
- Interferon-β induction heterogeneity during KSHV infection is correlated to levels and activation of the transcription factors ATF2 and RelA, and not IRF3.bioRxiv : the preprint server for biology · 2025Article
- A Review of Cross-Species Transmission Mechanisms of Influenza Viruses.Veterinary sciences · 2025Review
- The use of single-cell RNA-seq to study heterogeneity at varying levels of virus-host interactions.PLoS pathogens · 2024Review
- Type I Interferon, Induced by Adenovirus or Adenoviral Vector Infection, Regulates the Cytokine Response to Lipopolysaccharide in a Macrophage Type-Specific Manner.Journal of innate immunity · 2024Article
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- The role of exosomes from BALF in lung disease.Journal of cellular physiology · 2022Review
- Innate immune responses in RNA viral infection.Frontiers of medicine · 2021Review
- Viral and host heterogeneity and their effects on the viral life cycle.Nature reviews. Microbiology · 2021Review
- Influenza Viruses: Innate Immunity and mRNA Vaccines.Frontiers in immunology · 2021Review
- Microglial Implications in SARS-CoV-2 Infection and COVID-19: Lessons From Viral RNA Neurotropism and Possible Relevance to Parkinson's Disease.Frontiers in cellular neuroscience · 2021Review
- Single cell resolution of SARS-CoV-2 tropism, antiviral responses, and susceptibility to therapies in primary human airway epithelium.PLoS pathogens · 2021Article
- Virus-Intrinsic Differences and Heterogeneous IRF3 Activation Influence IFN-Independent Antiviral Protection.iScience · 2020Article
- Cell type- and replication stage-specific influenza virus responses in vivo.PLoS pathogens · 2020Article
- Single-Cell Virus Sequencing of Influenza Infections That Trigger Innate Immunity.Journal of virology · 2019Article
- Respiratory epithelial cells as master communicators during viral infections.Current clinical microbiology reports · 2019Article
- The dual role of innate immunity during influenza.Biomedical journal · 2019Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The innate host defense against influenza virus is largely dependent on the type I interferon (IFN) system. However, surprisingly little is known about the cellular source of IFN in the infected lung. To clarify this question, we employed a reporter mouse that contains the firefly luciferase gene in place of the IFN-β-coding region. IFN-β-producing cells were identified either by simultaneous immunostaining of lungs for luciferase and cellular markers or by generating conditional reporter mice that express luciferase exclusively in defined cell types. Two different strains of influenza A virus were employed that either do or do not code for nonstructural protein 1 (NS1), which strongly suppresses innate immune responses of infected cells. We found that epithelial cells and lung macrophages, which represent the prime host cells for influenza viruses, showed vigorous IFN-β responses which, however, were severely reduced and delayed if the infecting virus was able to produce NS1. Interestingly, CD11c(+) cell populations that were either expressing or lacking macrophage markers produced the bulk of IFN-β at 48 h after infection with wild-type influenza A virus. Our results demonstrate that the virus-encoded IFN-antagonistic factor NS1 disarms specifically epithelial cells and lung macrophages, which otherwise would serve as main mediators of the early response against infection by influenza virus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.